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Histopathology > Cardiac Histopathology > Flashcards

Cardiac Histopathology Flashcards

1
Q

Histological findings post MI

  1. Under 6hours
  2. 6-24 hours
  3. 1-4 days
  4. 5-10 days
  5. 1-2 weeks
  6. 2weeks+
A
  1. Under 6hours (normal histology, CK-MB also normal)
  2. 6-24 hours (loss of nuclei, homogenous cytoplasm, necrotic cell death).
  3. 1-4 days (infiltration of macrophages, peak troponin in at 24-48 hours)
  4. 5-10 days (removal of debris)
  5. 1-2 weeks (granulation tissue, new blood vessels, myofibroblasts, collagen synthesis)
  6. 2weeks+ (strengthening, decellularising scar tissue)
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2
Q

Complications of MI (4 main groups)

A
  1. Mechanical (e.g. CCF)
  2. Arrhythmias (e.g. VF)
  3. Pericardial (e.g. Peri-infarct associated pericarditis, pericardial effusion).
  4. Mural thrombus formation (can embolise)
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3
Q

5 main mechanical complications of MI

A
  1. Cardiogenic shock (contractile dysfunction due to loss of active muscle).
  2. CCF (due to ventr dysfunction and arrhythmias)
  3. LV infarct (papillary muscle dysfunction can lead to mitral regurg)
  4. Cardiac rupture (ventricular wall (haemopericardium), septum (left to right shunt), papillary muscle (mitral regurg)).
  5. Ventricular aneurysm (usually develops more than 1 month post MI).
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4
Q

main arrhythmic complication of MI

A
  1. VF (usually in first 24 hours, common cause of sudden death)

90% of patients develop an arrhythmia post MI.

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5
Q

Describe clinical features and the timespan of dressers syndrome.

A

Persistent low grade fever,
Chest pain (usually pleuritic)
Maybe pericardial effusion
Usually occurs 2-3 weeks post MI, but can be longer.

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6
Q

MI basic definition

A

Myocardial cell death due to prolonged ischaemia.

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7
Q

What is the difference between HFpEF and HFrEF

A

HFpEF- preserved ejection fraction. Diastolic heart failure. Ventricles do not relax properly to allow ventricular filling.

HFpRF- reduced ejection fraction. Systolic heart failure. Ventricles do not contract effectively to pump oxygenated blood around the body.

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8
Q

What are normal and abnormal ejection fraction percentages?

A

EF>75% indicates a hypertrophic cardiomyopathy.
Normal EF is usually 55-70%. However you can still have a normal ef, but HFpEF.
EF 40-55 indicates damage but may not be heart failure.
EF

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9
Q

Give 6 common causes of heart failure

A
  1. HTN
  2. Ischaemic heart disease
  3. Arrhythmias
  4. Valve disease
  5. Dilated cardiomyopathy
  6. Myocarditis
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10
Q

Give 6 clinical features of heart failure

A

Dyspnoea, orthopnoea, PND, wheeze, fatigue, RV failure, peripheral oedema

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11
Q

2 main causes of RV failure

A

LVF

Chronic severe pulmonary HTN

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12
Q

4 Heart failure investigations and findings?

A

BNP, CXR, ECG, echo

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13
Q

3 types of cardiomyopathy

A

Dilated (systolic dysfunction)

Hypertrophic (diastolic dysfunction)

Restrictive (diastolic dysfunction)

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14
Q

7 causes of dilated cardiomyopathy

A

Idiopathic, alcohol, peripartum, genetic, sarcoidosis, haemochromotosis, myocarditis

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15
Q

Causes of HCM

A

Genetic, glycogen storage diseases

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16
Q

Name 3 typical features of HCM

A
  1. Thick walled
  2. Heavy
  3. Hypercontractile

Histologically myocyte disarray.

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17
Q

3 causes of restrictive cardiomyopathy (connective tissues issues)

A

Sarcoidosis, amyloidosis, radiation induced fibrosis.

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18
Q

What is ARVC

A

Arrhythmogenic right ventricular cardiomyopathy

Myocyte loss with fibrofatty replacement typically affecting the RV.

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19
Q

What 4 main systems does acute rheumatic fever affect, and how?

A

Heart: pancarditis
Joints: arthiritis, synovitis
Skin: erythema marginatum
Neurological: encephalopathy, Sydenham’s chorea

20
Q

What is erythema marginatum?

A

Erythema (redness of the skin or mucous membranes) specifically involving pink rings on the torso and inner surfaces of the limbs which come and go for as long as several months. It is found primarily on extensor surfaces.

21
Q

What is the peak age of onset for acute rheumatic fever?

A

5-15 years

22
Q

How long after the initial infection does ARF develop?

A

2-4 weeks

23
Q

What is the most common infection for ARF to develop after?

A

Strep throat (lancefield group a strep)

24
Q

What are the 4 main clinical features of ARF

A

Fever, tachycardia, malaise, migrating polyarthralgia

25
Q

What is the pathology of ARF

A

Antigenic mimicry. Immune response to antigens from previous streptococcal infection cross-reacts with myocardial antigens.

26
Q

What are the 3 key findings on histology for ARF? Describe them.

A
  1. Beady fibrous vegetations (warty ‘verrucae’ found near valve leaflet closure lines)
  2. Aschoff bodies (small giant cell granulomas)
  3. Anitschkov myocytes (regenerating myocytes)
27
Q

What are the diagnostic criteria, tests, results and treatment of ARF?

A

Jones criteria, along with raised ESR and ASOT (anti-streptolysin O). Benzylpenicillin or erythromycin in penicillin allergic patients.

28
Q

What are the 4 main types of vegetative endocarditis

A
  1. Rheumatic heart disease
  2. Infective endocarditis
  3. Non-bacterial thrombotic endocarditis (Marantic)
  4. Libman-Sacks Endocarditis
29
Q

Describe the pathology and vegetation characteristics of infective endocarditis

A

Invasion of heart valves or mural endocardium by microbe.
Large irregular masses on valve cusps, extending into the chordae (chordae are like stringy valve tendons connecting to papillary muscle).

30
Q

Describe the pathology and vegetation characteristics of Non-bacterial thrombotic endocarditis (Marantic)

A

Caused by DIC/hypercoagulable states.

Small bland vegetations formed of thrombi are attached to valve leaflet closure lines

31
Q

Describe the pathology and vegetation characteristics of Libman-Sacks Endocarditis

A

Pathology unknown. Associated with immune disorders (SLE, Anti-phospholipid syndrome).
Small, sterile, platelet rich, warty vegetations.

32
Q

Basic Infective Endocarditis definition

A

colonisation or invasion of endocardium by pathogens (usually bacteria) causing an inflammatory response..

33
Q

Give 6 causes of infective endocarditis bacteraemia

A
  1. Poor dental hygiene.
  2. Dental treatments
  3. Soft tissue infection
  4. IVDU,
  5. Cannulae/lines
  6. Cardiac surgery/pacemakers
34
Q

Give 6 predisposing factors for infective endocarditis

A
  1. Rheumatic heart disease
  2. Mitral valve prolapse
  3. Calcified valves
  4. Bicuspid aortic valve
  5. Prosthetic valves
  6. Congenital defects
35
Q

Name 2 causative organisms for Acute and Subacute infective endocarditis

A

Acute: Staph aureus, Strep pyogenes
Subacute: Strep Viridans, Staph epidermis, Coxiella, Mycoplasma, Candida

36
Q

What is the difference in vegetation morphology and spread between acute and subacute infective endocarditis?

A

Acute: Larger and more localised lesions. Aortic spread.
Subacute: Smaller, friable soft lesions. Chordae spread.

37
Q

Give 10 clinical features of infective endocarditis (5 are more specific)

A

Fever, malaise, anaemia, rigors, splenomegaly

New murmur, roth spots (retinal hemorrhages with pale centres), osler’s nodes, janeway lesions, splinter hemorrhages

38
Q

What valves are usually affected in infective endocarditis?

A

Usually mitral or aortic.

UNLESS IVDU/cannula, etc. where right sided valves are involved

39
Q

What are the diagnostic criteria and treatment for infective endocarditis?

A

Duke’s criteria, benzylpenicillin and gentamycin

40
Q

What valves are usually involved in chronic rheumatic valve disease?

A

Mitral>Aortic>Tricuspid>Pulmonary

41
Q

What are the physical pathological signs of chronic rheumatic valve disease?

A

Thickening of valve leaflet. Thickening, shortening and fusion of chordae tendinae.

42
Q

What is the main cause of aortic stenosis?

A

Calcification. Process is sped up by the presence of a bicuspid valve

43
Q

What are the clinical signs of mitral valve prolapse on ausculatation?

A

mid-systolic click and late systolic murmur

44
Q

What are the 3 classifications of aortic regurgitation and their sub-groups?

A

Rigidity (rheumatic, degenerative)
Destruction (endocarditis)
Dilatation (valve is insufficiently large to cover the increased area.e.g. immune mediated issues, marfan’s dissecting aneurysm)

45
Q

What are the 5 main classifications of pericarditis

A
  1. Fibrinous (MI, uremia)
  2. Purulent (Staph)
  3. Granulomatous (TB)
  4. Hemorrhagic (tumour, TB, uremia)
  5. Constrictive (Fibrous, can be caused by any of the above.).

Histopathology (4 decks)

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